Serotonin and platelet activation during treatment with isradipine
Jazyk angličtina Země Spojené státy americké Médium print
Typ dokumentu časopisecké články
PubMed
1720482
Knihovny.cz E-zdroje
- MeSH
- agregace trombocytů účinky léků MeSH
- blokátory kalciových kanálů terapeutické užití MeSH
- dihydropyridiny terapeutické užití MeSH
- dospělí MeSH
- hypertenze krev farmakoterapie MeSH
- inhibitory agregace trombocytů terapeutické užití MeSH
- isradipin MeSH
- krevní tlak účinky léků MeSH
- lidé středního věku MeSH
- lidé MeSH
- lipoproteiny LDL farmakologie MeSH
- senioři MeSH
- serotonin krev farmakologie MeSH
- techniky in vitro MeSH
- trombocyty účinky léků metabolismus MeSH
- Check Tag
- dospělí MeSH
- lidé středního věku MeSH
- lidé MeSH
- senioři MeSH
- Publikační typ
- časopisecké články MeSH
- Názvy látek
- blokátory kalciových kanálů MeSH
- dihydropyridiny MeSH
- inhibitory agregace trombocytů MeSH
- isradipin MeSH
- lipoproteiny LDL MeSH
- serotonin MeSH
The effect of the calcium antagonist isradipine on serotonin metabolism and platelet aggregation was studied in 17 patients with essential hypertension. Platelet serotonin content, plasma serotonin, 5-hydroxyindoleacetic acid levels, and platelet aggregation [induced ex vivo by serotonin and low-density lipoprotein (LDL)] were measured after a 4-week placebo period and after 12 weeks of oral treatment with isradipine. Isradipine treatment significantly inhibited platelet aggregation induced by LDL and serotonin; the amplifying effect of LDL on serotonin-induced aggregation seen with placebo was not observed after 12 weeks of treatment with isradipine. Platelet serotonin content increased significantly during isradipine treatment; this increase was inversely related to the pretreatment content of serotonin in platelets. The results indicate that treatment with isradipine restores the impaired handling of platelet serotonin as well as the platelet response to serotonin and LDL in hypertensive patients. This effect of isradipine may be regarded as one of the cellular mechanisms of thrombovascular protection and may be of clinical significance in terms of platelet and vessel wall interaction.